Group Presentations Flashcards
Stroke volume
SV = EDV - ESV
Cardiac output
CO = Stoke volume x HR
Changes in HR will greater effect CO.
- HR may increase 100-200% with exercise
- stroke volume may increase <50%
Normal CO of adult at rest = 5-6 L/min
Cardiac index
-normalizes CO to individuals of different sizes
CI = CO/BSA
Normal CI = 2.6 - 4.2 L/min/m2
How does increasing HR affect CO?
-stroke volume falls as HR increases due to decrease ventricular filling
What are some mechanisms that cause stroke volume to increase despite increased HR and decreased filling time?
- Anrep effect: abrupt increase in afterload can cause a modest increase in inotropy
- Treppe (Bowditch effect): when HR is elevated Ca++ doesn’t have time to completely leave cell. The increase of Ca++ sitting on actin and myosin causes a stronger squeeze, increasing contractility with high HR
Preload
- initial stretching of the cardiac myocytes prior to contraction; therefore is related to sarcomere length at the end of diastole
- sarcomere length difficult to determine, indirect indices are used
- EDV and EDP
How does ventricular compliance affect preload?
Decreased compliance: decreased volume at higher pressure
Increased compliance: higher volumes at lower pressure
-compliance is the ratio of change in volume/change in pressure
Frank-Starling mechanism
-stretched fibers recoil harder
What determines ventricular preload?
—increases preload—
- increased venous pressure
- ventricular compliance: greater compliance = greater filling and greater preload
- increased outflow resistance (pulmonary valve stenosis, pulmonary HTN) impairs ventricular emptying and increases preload
- decreased ventricular inotropy (ventricular failure)
-atrial contraction: normally small contribution. Sympathetic innervation enhances force of contraction at higher heart rates enhancing ventricular filling
—decreases preload—
-heart rate: HR and ventricular filling are inversely related
-inflow resistance: increase in this decreases preload
Afterload
- the “load” against which the heart must contract
- mainly aortic pressure
- aortic valve stenosis
- ventricular dilation
- the greater the pressure the greater the afterload and the less CO
- afterload decreases velocity of fiber shortening
-increased afterload = increased cardiac workload
Inotropy
- length-independent activation of contractile proteins
- an inotrope is any mechanism that alter myocin ATPase activity at a given sarcomere length alters force generation
- most inotropes involve Ca++
What increases contractility?
- catecholamines
- HR (bowditch/treppe effect)
- afterload (anrep effect)
What decreases contractility?
- parasympathetic innervation
- systolic failure
Systemic vascular resistance (SVR)
- resistance to blood flow offered by all systemic vasculature
- associated with LV afterload, but not synonymous
SVR = (MAP-CVP)
—————- x80
CO
Normal SVR = 900-1200 dynes/sec/cm5
Determinants of SVR
- arteriolar tone is primary determinant of SVR
- vessels in the systemic system are more compliant than in the pulmonary vascular system
What causes elevated SVR?
-mechanisms that cause vasoconstriction increase SVR
- sympathetic activation
- hypovolemia
- hemorrhagic or cardiogenic shock
- vasoconstricting drugs
What reduces SVR?
-mechanisms that cause vasodilation decrease SVR
- septic shock
- vasodilation medications
- parasympathetic stimulus
- hypercarbia
Systemic vascular resistance index
SVRI = (MAP - CVP)
______________ x80
CI
Commonly used to offer guidance in the use of vasoconstrictors or vasodilators
Pulmonary vascular resistance
- reflects blood flow through the pulmonary circulation. Resistance is influence by pulmonary capillaries and arteries
- if PVR high, right ventricle must work harder to move blood past pulmonic valve. Will lead to dilation of RV
PVR = (MPAP - PAWP)
———————- x80
CO
Normal PVR = 100 - 200 dynes/sec/cm5
Factors that increase PVR
- vasoconsticting drugs
- hypoxemia
- acidemia
- hypercapnia
- atelectasis
- hypovolemia
- hyperinflation (increased PEEP, increases PIP)
- sympathetic stimulation
- high Hct
- alpha-adrenergic agonists
Factors that decrease PVR
- vasodilating drugs
- alkalemia
- hypocapnia
- strenuous exercise
- block sympathetic stimulation (narcotics)
- low Hct
- alpha adrenergic antagonists
Pulmonary vascular resistance index
-PVRI = (MPAP-PAWP)
—————— x80
CI
SVO2
- O2 saturation of the blood returning to the right side of the heart.
- it is the measurement of the relationship between O2 consumption and O2 delivery in the body
- normal = 60-80%
What causes low SVO2?
- <60%. O2 supply is insufficient or the O2 demand has increased
- decreased Hgb
- decreased SaO2 (hypoxemia)
- any form of shock or arrhythmia
What causes high SVO2?
- > 80%. O2 demand has declined or the O2 supply had increased
- increased O2 delivery
- decreased O2 demand (hypothermia, anesthesia, neuromuscular blockade)
- high flow states: sepsis, hyperthyroidism, severe liver disease
Einthoven’s law
- if the ECGs are recorded simultaneously with the 3 limb leads, the sum of the potentials recorded in leads I and III will equal the potential in lead II
- Lead I potential + Lead III potential = Lead II potential
What is most useful lead in detecting cardiac arrhythmia?
Lead II as it lies close to cardiac axis
Benefit to lead V1?
- distinguish between LV ectopy and RV ectopy
- can tell right BB from left BB
- p waves are more easily seen in right sided monitoring leads
- differentiation of SVT and vtach
Wilson’s Central Terminal Theory
-serves as a reference point for each of the 6 electrodes in 12 lead EKG
How could you look at posterior heart with EKG?
V6—>V9
V5—>V8
V4—>V7
What are 2 main coronary arteries that supply the heart?
Left and right coronary arteries
- originate in the aorta, immediately superior to the aortic valve
- perfused during diastole
Left coronary artery supplies what?
- Anterior left ventricle
- Left lateral portion of left ventricle
Divides into:
- Left anterior descending: supplies anterior and septal regions of the heart
- including LV, interventricular septum, and parts of RV
- Left circumflex: supplies lateral portions of the heart
- including left atrium and LV
Right coronary artery supplies what?
- Right atrium
- Most of the right ventricle
- Posterior part of left ventricle (in 80-90% of population)
Divides into:
- Right martial artery: supplies right atrium and RV
- posterior descending artery: supplies the bottom portion of LV and back of septum (in conjunction with left circumflex)
ST elevation
-elevation >0.5-1mm in 2 or more contiguous precordial leads, or 2 mor more adjacent limb leads
What is seen with posterior wall ischemia/infarct?
- ECG changes will be reversed as will be looking at the endocardial surface of the posterior heart wall
- initially ST segments V1 and V2 are depressed
- ST elevation in leads V7, V8, and V9
- RCA (PDA) and/or LCX involved
- rarely seen by itself
Contraindications to fibrinolytic therapy
- SBP>180
- DBP>110
- right arm vs left arm BP difference >15
- stoke >3 hours or < 3 months
- Hx of structural CNS disease
- head/facial trauma within 3 weeks
- major trauma (GI bleeding/surgery within 4 weeks)
- taking blood thinners
- pregnancy
- Hx intercranial hemorrhage
- advanced cancer, sever liver/renal disease
Time goals for reperfussion therapies
- balloon inflation PCI: door to inflation goal 90 min
- fibrinolysis: door to needle goal 30 min
What do you do if ST elevation during surgery?
*mange causes of decreased O2
- tachycardia
- hypotension
- decreased O2
- anemia
- manage causes of increased O2 demand
- tachycardia
- increase preload
- increased contractility
- increased afterload
What is CVP?
Central venous pressure
- direct measurement of the blood pressure in the right atrium and vena cava
- tip of the catheter rests in the lower third of the superior vena cava
What are the 3 ports of a pulmonary artery catheter?
- Proximal: (CVP) port measures right atrial and central venous pressures
- Distal port measures pulmonary artery pressure and wedge pressure when a balloon is inflated
- Thermistor port is connected to the monitor to give continuous temp readings
CVP measurement
- normal 1-10 mmHg
- measured at the end of expiration, this is when pleural pressure are approximately equal to atmospheric pressure (unless using PEEP)
Waveform of CVP
- a wave: contraction of RA
- c wave: closure of tricuspid valve and contraction of ventricles
- v wave: passive filling of RA
- x descent: drop in atrial pressure during ventricular systole caused by atrial relaxation
- y descent: atrial pressure drop as blood enters the ventricle during diastole (early ventricular filling)
What can cause abnormal CVP waveforms?
- malpositioning of catheter
- dysrhythmias
- atrial fibrillation
- junctional rhythms
- premature ventricular contractions
-valvular defects also produce dramatic changes in CVP, causing increase in amplitude of the v wave
What causes “cannon” a waves or giant a waves?
- junctional rhythms
- complete AV block
- PVCs
- ventricular pacing
- tricuspid or mitral stenosis
- diastolic dysfunction
- myocardial ischemia
- ventricular hypertophy
What causes loss of a waves or only v waves on CVP?
- a-fib
- v-pacing in the setting of asystole
What causes large v waves on CVP?
- tricuspid or mitral regurgitation
- acute increase in intravascular volume
Causes of low CVP?
-hypovolemia
Causes of higher CVP
- higher PEEP settings
- PEEP of 10 cm H2O usually results in increase of CVP by 3 cmH2O
- RV failure
- tricuspid stenosis or regurgitation
- cardiac tamponade
- constrictive pericarditis
- volume overload
- pulmonary HTN
- LV failure (chronic)
Where is proper placement of PA cath?
- 2cm left of mediastinal border
- zone 3 of lungs is the optimal location
- tip of the cath sits in the pulmonary artery
Pulmonary artery pressures
- normal PAP = 15-25/5-15
- dicrotic notch is the usual feature of the PA waveform and represents aortic valve closure
MPAP: is the average pressure in the pulmonary vasculature throughout the cardiac cycle
Mean arterial pressure
MAP = SVR x CO MAP = DBP + (SV/3)
Korotkoff sounds
-these sounds appear and disappear as the BP cuff is inflated and deflated
Auscultation vs oscillometric BP reading
- both can be taken manually
- either by listening or by watching oscillometric variation of on sphygmomanometer
-automatic machines use oscillometric variation to read pressures
Contraindications of a-lines
-pt with compromised arterial supply such as pts with Reynolds or thromboangitis obliterans (Buerger’s disease)
What are signs of possible hypovolemia in vented pt with a-line?
-the more hypovolemc a pt is, the greater the inspiratory decrease of SBP and stroke volume
What do the different colors of color Doppler represent?
- blue: away from transducer
- red: towards transducer
- green/mosaic: turbulent flow
What are the main recommended cuts for TEE?
- 20 cuts/views determined by The American Society of Echocardiography (ASE) and The Society of Cardiovascular Anesthesiologists (SCA)
- est a systemiztion of TEE
Uses of TEE during cardiac and thoracic surgery
- confirm and refine pre-op diagnosis
- detect more or unsuspected pathology
- adjust the anesthetic and surgical plan accordingly
- assess the results of surgical intervention
What are some things that intro-op TEE can assess for?
- assessment of hemodynamic instability
- valvular assessment
- monitoring myocardial ischemia
- detention of aortic atheromatous plaques
- aortic dissection
- congenital cardiopathy
- detection intracardiac air
Contraindications of TEE
- esophageal stenosis
- large esophageal diverticuli
- recent esophageal surgery/sutures
- know esophageal interruptions
What are the 3 fundamental processes of thermoregulation?
- Afferent sensing: receptors throughout body send info to hypothalamus
- Central control: hypothalamus primary center for them control. Calculated response is made from eh afferent signal
- Efferent response: sends calculated response to targeted functions systems within the body
What are actions that can help with temperature control of pt?
- prewarming pt
- room conditions
- warming IV fluids
- warming blanket
What are some effects of hypothermia?
- cardiac arrhythmias and ischemia
- increased peripheral vascular resistance
- left-shift of the hemoglobin-oxygen saturation curve
- reversible coagulopathy
- altered mental status
- impaired renal function
- delayed drug metabolism
- impaired wound healing
- increased risk of infection
How do anesthetics interfere with central thermoregulation?
- all inhaled agents cause vasodilation
- spinal/epidural: vasodilation and altered perception of temp
- general: vasodilation and redistribution
- opioids: depress sympathetic outflow
What are the 3 phases of intra-op hypothermia?
- Phase 1: core temp decreases 1-2 degrees C during 1st hour of general anesthesia
- anesthetic induced vasodilation
- heat shifts from central compartments
- little heat loss from pt to environment
- Phase 2; gradual decline in core temp (hours 3-4 of surgery)
- continuous heat loss from pt to environment
- heat loss = metabolic heat production ???
- Phase 3: when core temp reaches a point of steady state
What is malignant hyperthermia (MH)?
-rare hyperametabolic disease following exposure to inhaled General anesthetics or succinylcholine
-presents within minutes up to 1 hour after triggering anesthetic
Causes:
-mutation of Ryr1 receptor located on chromosome 19
-mutations involving sodium channel of chromosome 17
-autosomal recessive form of MH has been associated with king-Denborough syndrome
What are signs and symptoms of MH?
- increased CO2
- increased sympathetic activity
- markedly increased metabolism
- hyperthermia
What drugs are known to trigger MH?
- inhaled anethetics
- ether
- halothane
- methoxyflurane
- enflurane
- isoflurane
- desflurane
- sevoflurane
- depolarizing muscle relaxant
- succinylcholine
What other conditions to consider if pt exhibiting some symptoms of MH?
- NMS
- thyroid storm
- pheochromocytoma
- drugs-induced hyperthermia
- environmental hyperthermia
- brain injury
- sepsis
- transfusion reaction
What is the treatment of MH?
- stop triggering agents
- hyperventilate/100% O2
- Dantrolene (2.5mg/kg)
- bicarbonate
- glucose and insulin
- IVF and cooling blanket
- fluid output monitoring and furosemide
- fast heart (tachycardia)
